ROLE OF RESIDUAL INSULIN-SECRETION IN PROTECTING AGAINST KETOACIDOSIS IN INSULIN-DEPENDENT DIABETES

The role of preserved beta-cell function in preventing ketoacidosis in type I insulin-dependent diabetes was assessed in eight patients with and seven patients without residual beta-cell function as determined from C-peptide concentrations. After 12 hours of insulin deprivation blood glucose, ketone-body, non-esterified fatty-acid, and glycerol concentrations were all significantly higher in patients without beta-cell function than in those with residual secretion. Mean blood glucose concentrations reached 17.2±SE of mean 1.3 mmol/l (310 ±23 mg/100 ml) in the first group compared with 8.8±1.4 mmol/l (159±25 mg/100 ml) in the second (P<0.01), while 3-hydroxybutyrate concentrations rose to 5.5±0.5 mmol/l (57±5 mg/100 ml) and 1.4±0.3 mmol/l (15±3 mg/100 ml) in the two groups respectively (P<0.01). Individual mean C-peptide concentrations showed a significant inverse correlation with the final blood glucose values (r= −0.91; P<0.02). These findings strongly suggest that even minimal residual insulin secretion is important for metabolic wellbeing in diabetes and may prevent the development of severe ketoacidosis when insulin delivery is inadequate. © 1979, British Medical Journal Publishing Group. All rights reserved.